ESC Guidelines on the diagnosis and treatment of peripheral artery ...

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In general, the risk factors for carotid stenosis are similar to
those for LEAD, although smoking, while commonly associated
with carotid disease, is not so dominant as with LEAD. Several
population-based studies have found in both symptomatic and
asymptomatic disease that the classic risk factors of smoking,
high low-density lipoprotein (LDL) cholesterol, low HDL cholesterol,
hypertension, and diabetes mellitus are associated with
higher risk in both men and women irrespective of age. 9 – 11 The
risk factors for carotid artery disease, however need to be distinguished
from those for ischaemic stroke, which is not necessarily
related to stenosis in the carotid arteries.
Likewise, for atheromatous renal artery disease the pathogenesis
is similar to that seen in other vascular sites and, although the evidence
is limited, would appear to be associated with typical cardiovascular
risk factors. 21 These include pre-existing high blood
pressure in which the hypertension is not necessarily a complication
but may be a cause of the RAS and may partly explain
why in many patients revascularization may not lead to a reduction
in blood pressure.
In chronic mesenteric artery disease, the atheromatous lesions
normally occur in the proximal segments of the splanchnic arteries.
The frequency of diffuse atherosclerosis has not been well
described but would appear to occur mostly in patients with endstage
renal disease (ESRD) or diabetes. The classic cardiovascular
risk factors appear to be important, although hypocholesterolaemia
(rather than hypercholesterolaemia) may be a presenting
finding due to a patient’s chronic malnourished state.
Significant associations were found between both increasing age
and higher systolic blood pressure with the presence of upper
extremity artery disease (UEAD). 15 Compared with never
smokers, the risks were increased in current and past smokers,
and the odds ratio (OR) of 2.6 for current smokers was the
highest of any risk factor, perhaps mirroring that found for
LEAD. While a higher HDL cholesterol level appeared to be protective,
surprisingly no association was found between total
cholesterol and subclavian stenosis. Diabetes mellitus was also
not related, although in another study the prevalence of UEAD
was found to be slightly higher in diabetic compared with nondiabetic
patients. 22 Interestingly, in the four cohort study, LEAD,
compared with CAD and cerebrovascular disease, was much
more strongly related to UEAD. 15
3.3 General diagnostic approach
3.3.1 History
History of risk factors and known co-morbidities is mandatory.
Hypertension, dyslipidaemia, diabetes mellitus, smoking status, as
well as history of CVD must be recorded. Medical history should
include a review of the different vascular beds and their specific
symptoms:
† Family history of CVD.
† Symptoms suggesting angina.
† Any walking impairment, e.g. fatigue, aching, cramping, or pain
with localization to the buttock, thigh, calf, or foot, particularly
when symptoms are quickly relieved at rest.
† Any pain at rest localized to the lower leg or foot and its association
with the upright or recumbent positions.
<strong>ESC</strong> <strong>Guidelines</strong>
† Any poorly healing wounds of the extremities.
† Upper extremity exertional pain, particularly if associated with
dizziness or vertigo.
† Any transient or permanent neurological symptom.
† History of hypertension or renal failure.
† Post-prandial abdominal pain and diarhoea, particularly if related
to eating and associated with weight loss.
† Erectile dysfunction.
This cannot be an exhaustive list, and a review of symptoms should
include all domains. It is important to emphasize that history is a
cornerstone of the vascular evaluation.
One should remember that many patients, even with advanced
disease, will remain asymptomatic or report atypical symptoms.
3.3.2 Physical examination
Although physical examination alone is of relatively poor sensitivity,
specificity, and reproducibility, a systematic approach is mandatory.
It must include at least:
† Measurement of blood pressure in both arms and notation of
inter-arm difference.
† Auscultation and palpation of the cervical and supraclavicular
fossae areas.
† Palpation of the pulses at the upper extremities. The hands must
be carefully inspected.
† Abdominal palpation and auscultation at different levels including
the flanks, periumbilical region, and the iliac regions.
† Auscultation of the femoral arteries at the groin level.
† Palpation of the femoral, popliteal, dorsalis pedis, and posterior
tibial sites.
† The feet must be inspected, and the colour, temperature, and
integrity of the skin, and the presence of ulcerations recorded.
† Additional findings suggestive of LEAD, including calf hair loss
and skin changes, should be noted.
Beyond their diagnostic importance, clinical signs could have a
prognostic value. A meta-analysis published in 2008 emphasized
the prognostic value of carotid bruit. 23 People with carotid
bruits have twice the risk of myocardial infarction and cardiovascular
death compared with those without. This predictive value can
be extended to other clinical signs, such as femoral bruit, pulse
abnormality in the lower extremity, or inter-arm blood pressure
asymmetry. All of these abnormalities can be an expression of subclinical
vascular disease.
3.3.3 Laboratory assessment
The aim of the laboratory assessment is to detect major risk
factors of CVD. The assessment should be performed according
to the <strong>ESC</strong> <strong>Guidelines</strong> on Cardiovascular Disease Prevention 24
and the <strong>ESC</strong>/EAS <strong>Guidelines</strong> for the Management of
Dyslipidaemias. 25
3.3.4 Ultrasound methods
3.3.4.1 Ankle–brachial index
The ABI is a strong marker of CVD and is predictive of cardiovascular
events and mortality. Low ABI values (,0.90) are predictive
of atherosclerosis, such as CAD and carotid artery disease. A
reduced ABI has been associated in several studies with an